Fluid bolus correct in this scenario?

[rhan101277]

55 y/o pt c/c of rectal bleeding, states "severe", happened during bowel movement and pt has hx of such. Pt takes no meds, has hx of GI bleeds and no allergies. Upon arrival pt is sitting on couch with a towel under him. Pt is diaphoretic and complains of weakness. States bleeding started about an hour ago and he bled "a lot". Pt reports some abdominal discomfort, abdomen is soft non-distended. Pedal pulses equal bilaterally but thready, same as radial. Pt vitals are as follows:

Sp02: 94% room air
Pulse: 130 thready
B/P: 143/80
Cap refill: 4 seconds

Pt placed on 12L NRB until further assessment can be done in the unit, Sp02 is 100% now. We have protocols that say for trauma to give 250cc increments fluid bolus to achieve SBP of greater than 90 systolic, max 2L. Medical shock protocols say initiate a fluid bolus is s/s of shock exists but further states that hypotension will be considered 90 systolic or less.

This patient looks bad and exhibits other signs besides blood pressure indicating he is in shock. He is clearly in compensated shock, but I am concerned it is trending toward decompensated. His heart rate is 110 in the unit and blood pressure 122/84. I go ahead and give him a 250cc bolus and then TKO. Blood pressure and heart rate un-affected. I am just concerned about letting someone decompensate to the point of irreversible shock. In the younger population (90 systolic) makes since but what about the elderly and folks with a hx of heart issues etc.

Thoughts?

 

[mycrofft]

Going to need prompt transport. I'd start the line and run in a fluid (what's the best here, folks?) but mostly as a means of keeping a vein open with incidental restoration of circulating volume for the length of the short ambulance run.

If you were in Bisonbeard Wyoming or something, an hour out, I'm not sure. Certainly try for a more extensive hx.

 

[Veneficus]

one of my favorite topcs.

55 y/o pt c/c of rectal bleeding, states "severe", happened during bowel movement and pt has hx of such. Pt takes no meds, has hx of GI bleeds and no allergies. Upon arrival pt is sitting on couch with a towel under him. Pt is diaphoretic and complains of weakness. States bleeding started about an hour ago and he bled "a lot". Pt reports some abdominal discomfort, abdomen is soft non-distended. Pedal pulses equal bilaterally but thready, same as radial. Pt vitals are as follows:

Sp02: 94% room air
Pulse: 130 thready
B/P: 143/80
Cap refill: 4 seconds

Pt placed on 12L NRB until further assessment can be done in the unit, Sp02 is 100% now. We have protocols that say for trauma to give 250cc increments fluid bolus to achieve SBP of greater than 90 systolic, max 2L. Medical shock protocols say initiate a fluid bolus is s/s of shock exists but further states that hypotension will be considered 90 systolic or less.

This patient looks bad and exhibits other signs besides blood pressure indicating he is in shock. He is clearly in compensated shock, but I am concerned it is trending toward decompensated. His heart rate is 110 in the unit and blood pressure 122/84. I go ahead and give him a 250cc bolus and then TKO. Blood pressure and heart rate un-affected. I am just concerned about letting someone decompensate to the point of irreversible shock. In the younger population (90 systolic) makes since but what about the elderly and folks with a hx of heart issues etc.

Thoughts?

First off, using "compensated, decompensated and irreversible shock" is really better for pathologists than clinical guidance.

Chystaloid will only demonstrate response in class I or Class II shock as defined by the American College of Surgeons.

The point of theraputic hypotension is to prevent dilution of clotting mechanisms (platelet and clotting cascade) as well as to help maintain a higher extravascular pressure compared to intravascular. (the physical mechanism behind hemostasis)

It is commonly accepted that the osmotic and volume shift that happens in shock will generally cause the 3rd spacing of around 500cc of chrystaloid.

So you will unlikely see a response from such a low dose.(used the word dose on purpose)

I would divide clinical shock into early and late phase (a system used in both surgery and anesthesia texts) Since EMS does not deal with shock outside of delivery of O2, it will be helpful to think of the mechanisms and purpose of chrystaloid.

It will not increase heme concentration.

It will lower hematocrit

(those are 2 of the 3 main mechanisms of Do2.)

It will increase circulating volume and hopefully cardiac output.

To be effective, you may have to give a more substantive fluid bolus and see if it worsens bleeding. If it does, I would stop it early.

If it helps normalize vitals without an increase in bleeding I would call it a win, as it didn't clinically affect hemostasis.

If you gave 250 an nothing happened, I wouldn't be surprised or concerned by that news at all.

In class I and II of shock, chrystaloid is still an indicated treatment. There is some disagreement on whether or not that assumes hemostasis or not. In my mind it does, but it is a point of contention depending on who you ask.

Obviously you have to follow protocols and my musings on this should direct your concerns to your medical director, not change your practice, but it looks to me like they wrote a rather mindless protocol in order to remove decision making and be conservative enough to accept hypotension for a time instead of risking the improper application of volume replacement therapy.

"a lot of blood" means different things to different people. You should at least try to estimate it, even though it is often hard to do.

 

[AlphaButch]

Given the info, I'd run a line TKO but would withhold fluids (although I would be stuck with a 250cc challenge in this case if I had your protocols - hypotensive at 90 SBP). With the hx of bleeds, I'd try to do everything to limit reducing the patient's clotting ability - titrating fluid if necessary to maintain a base pressure for perfusion. There isn't anything I can do about an internal bleed other than maintain pressure the best I can and rapid transport, adding more fluid than is necessary will just give the patient more to bleed into their peritonial cavity (most likely suspect, or wherever the fluid is going) and/or turn their blood into kool aid.

Transport time would affect my decision in this alot. Greater than 30 minutes, I'd have two lines in if possible (one TKO saline, one LR bolus then titrated to maintain pressure unless it exacerbates the situation).

 

[Veneficus]

I think the questions of the hour are:

Was he actively bleeding when you found him?

How much?

 

[mycrofft]

Was the blood ORIGINATING from the colon, or the rectum/anus? If the latter, a packing could actually show it/help. But I don't know how field EMS would determine, so, disregard unless someone writes a blanket order for rectal packing.

Bet Johnny and Roy never did THAT.

 

[Veneficus]

Was the blood ORIGINATING from the colon, or the rectum/anus? If the latter, a packing could actually show it/help. But I don't know how field EMS would determine, so, disregard unless someone writes a blanket order for rectal packing.

Bet Johnny and Roy never did THAT.

If he has a history, he has a dx.

 

[rhan101277]

Well I had hid sit on a trauma dressing. He wasn't dripping blood so it must have clotted off. Yes I was concerned about diluting clotting factors with a fluid bolus, but it was a very small one. He was still compensated at destination.

Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 176. ISBN 0-07-148480-9.

When Permissive Hypotension Should be Avoided

Patients with preexisting hypertension are at higher risk of death and morbidity during permissive hypotension. This is due to the shift in the autoregulatory curve to the right for hypertensive patients.
Permissive hypotension relies on the heart's ability to pump fluid through the body efficiently. Less intravascular fluid results in a less fluid filling the heart (lower end diastolic volume) which results in a lower amount of volume pumped out of the heart (stroke volume). This is based on the frank-starling law of the heart. Healthy patients are able to compensate for lower volumes Patients with preexisting cardiovascular disease that limits myocardial function such as angina pectoris and preexistence of cardiovascular disease limits the use of this concept. This can result in limited coronary perfusion and resulting ischemic damage to the heart and potentially a myocardial infarction (heart attack).[9]
This concept may also be an issue in cerebrovascular disease and carotid artery stenosis; compromised renal (kidney) function in certain conditions, where low blood pressure may induce sludge (thickening of blood) and lead to occlusion of the vessel lumen.
In a high percentage of polytraumatized patients the brain is also affected. The results from the Traumatic Coma Data Bank show the influence of the presence or absence of hypotension (defined as one or more recordings of a systolic blood pressure ≤90 mm Hg) or hypoxia (PaO2 <60 mm Hg) at the time of admission on the outcome of patients who suffer traumatic brain injury and hypotension at admission to the hospital showed twice the mortality and a significant increase in morbidity when compared with patients who were normotensive. The concomitant presence of hypoxia and hypotension upon admission resulted in a 75% mortality.[10] Evidence strongly suggests that the avoidance or minimization of hypotension during the acute and postinjury period following traumatic brain injury had the highest likelihood of improving outcomes of any one single therapeutic maneuver.[11]

 

[FLdoc2011]

A 250cc bolus isn't going to make or break anything here.

The main thing here IMHO, which was already mentioned, is if he's still bleeding. If not actively bleeding and vitals/mentation staying where they are then I'm ok with holding off on aggressive prehospital fluids.

I think most of the delayed resuscitation/controlled hypotension stuff is based on trauma literature and is still controversial.

 

[Veneficus]

I think most of the delayed resuscitation/controlled hypotension stuff is based on trauma literature and is still controversial.

I think it is like anything else, it depends more on who is doing it, in what patient and what the goal is.

Everything I have seen on it is based on trauma, but the idea dates back to France circa 1914.

 

[Akulahawk]

55 y/o pt c/c of rectal bleeding, states "severe", happened during bowel movement and pt has hx of such. Pt takes no meds, has hx of GI bleeds and no allergies. Upon arrival pt is sitting on couch with a towel under him. Pt is diaphoretic and complains of weakness. States bleeding started about an hour ago and he bled "a lot". Pt reports some abdominal discomfort, abdomen is soft non-distended. Pedal pulses equal bilaterally but thready, same as radial. Pt vitals are as follows:

Sp02: 94% room air
Pulse: 130 thready
B/P: 143/80
Cap refill: 4 seconds

Pt placed on 12L NRB until further assessment can be done in the unit, Sp02 is 100% now. We have protocols that say for trauma to give 250cc increments fluid bolus to achieve SBP of greater than 90 systolic, max 2L. Medical shock protocols say initiate a fluid bolus is s/s of shock exists but further states that hypotension will be considered 90 systolic or less.

This patient looks bad and exhibits other signs besides blood pressure indicating he is in shock. He is clearly in compensated shock, but I am concerned it is trending toward decompensated. His heart rate is 110 in the unit and blood pressure 122/84. I go ahead and give him a 250cc bolus and then TKO. Blood pressure and heart rate un-affected. I am just concerned about letting someone decompensate to the point of irreversible shock. In the younger population (90 systolic) makes since but what about the elderly and folks with a hx of heart issues etc.

Thoughts?

Given what I bolded above, I'd be thinking start with a lower flow O2 and titrate up from there. Is he known to be actively bleeding now? That's something I'd want to know. Get him off the towel and put him on a clean pad. Bleeding "a lot" is descriptive but not quantitative. I'd start an IV, large-ish bore, and keep it TKO for now. He's clearly in a shock state but not to the point where I really start worrying. How's his mentation? He looks to me like someone that I would prepare to begin aggressive tx, but hold off until something tells me he needs it. I don't want to increase his BP back to where he starts popping clots and starts bleeding again. I don't want to dilute whatever clotting factors that are left-over if I don't have to. The fact that he's got present radial and pedal pulses says to me that he's got sufficient circulating volume that his body doesn't have to start seriously closing off more distal locations, though his cap refill time is slightly long, but still present.

He's got a Hx of GI bleeds. Has he had bleeds like this before? What was the outcome? To dredge up an old acronym, he just needs VOMIT.

V: got'em, recheck relatively frequently for decompensation signs - I engage in conversation to track mental status continually.
O: Low flow and titrate PRN to maintain SpO2 >94% (some protocols I've seen say 92%, from memory)
M: mostly used along with the (V) for earlish signs of decompensation - HR going up
I: Large-ish bore (18ga or higher) TKO in prep for more aggressive resuscitation / fluid / blood replacement later.
T: Get him rolling to the ED safely/quickly/quietly. He's not a Code 3 return, but unnecessary delay slows down his arrival at definitive care.

 

[Veneficus]

Well I had hid sit on a trauma dressing. He wasn't dripping blood so it must have clotted off. Yes I was concerned about diluting clotting factors with a fluid bolus, but it was a very small one. He was still compensated at destination.

Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 176. ISBN 0-07-148480-9.

When Permissive Hypotension Should be Avoided

Patients with preexisting hypertension are at higher risk of death and morbidity during permissive hypotension. This is due to the shift in the autoregulatory curve to the right for hypertensive patients.
Permissive hypotension relies on the heart's ability to pump fluid through the body efficiently. Less intravascular fluid results in a less fluid filling the heart (lower end diastolic volume) which results in a lower amount of volume pumped out of the heart (stroke volume). This is based on the frank-starling law of the heart. Healthy patients are able to compensate for lower volumes Patients with preexisting cardiovascular disease that limits myocardial function such as angina pectoris and preexistence of cardiovascular disease limits the use of this concept. This can result in limited coronary perfusion and resulting ischemic damage to the heart and potentially a myocardial infarction (heart attack).[9]
This concept may also be an issue in cerebrovascular disease and carotid artery stenosis; compromised renal (kidney) function in certain conditions, where low blood pressure may induce sludge (thickening of blood) and lead to occlusion of the vessel lumen.
In a high percentage of polytraumatized patients the brain is also affected. The results from the Traumatic Coma Data Bank show the influence of the presence or absence of hypotension (defined as one or more recordings of a systolic blood pressure ≤90 mm Hg) or hypoxia (PaO2 <60 mm Hg) at the time of admission on the outcome of patients who suffer traumatic brain injury and hypotension at admission to the hospital showed twice the mortality and a significant increase in morbidity when compared with patients who were normotensive. The concomitant presence of hypoxia and hypotension upon admission resulted in a 75% mortality.[10] Evidence strongly suggests that the avoidance or minimization of hypotension during the acute and postinjury period following traumatic brain injury had the highest likelihood of improving outcomes of any one single therapeutic maneuver.[11]

From Miller's Anesthesia, 7th edition, chapter 72, management of hypovolemia with TBI.

The most challenging of all trauma patients are those with severe TBI and coexisting hemorrhagic shock. A single episode of hypotension, defined as systolic blood pressure lower than 90 mm Hg, is associated with an increase in morbidity and doubled mortality after severe TBI.[147] Hypotension together with hypoxia is associated with a threefold increase in mortality. Systolic blood pressure less than 90 mm Hg should be avoided, with a goal of greater than 70 mm Hg MAP until ICP monitoring is instituted and CPP can be directly targeted. Contrary to practices in the past, current recommendations are to maintain a patient with severe TBI in a euvolemic state. Therefore, fluid resuscitation is the mainstay of therapy, followed by vasoactive infusions as needed. The ideal fluid has not yet been identified, but increasing evidence suggests that hypertonic saline solutions are optimal. Correction of anemia from blood loss is the first priority, with a goal of maintaining the hematocrit at greater than 30%. After the initial ABCDE management of a patient with severe TBI, a stepwise approach to maintenance of CPP is initiated, with a currently recommended goal range of 50 to 70 mm Hg, as discussed in Chapter 63.

In patients without TBI:

Chapter 54

Intravascular Volume Resuscitation of Patient in Hemorrhagic Shock

The urgent priorities for the resuscitation of a seriously bleeding patient are (1) ensuring an adequate airway, (2) ensuring adequate respiration, and (3) supporting the circulation. Stopping blood loss is most often achieved through manual pressure on the bleeding site or operative intervention (rarely arterial tourniquet application), or both. Formerly, intravenous crystalloid (United States) or colloid (Europe) solution was administered to normalize blood pressure. More recently, such intravenous fluids have been administered at rates just sufficient to maintain arterial systolic blood pressure between 80 and 100 mm Hg (with some centers limiting total infused volume during emergency medical services transport to 1 to 2 L of balanced salt solution [permissive hypotension]).[86] Benefits of this approach (achieved at the expense of non–vital organ hypoperfusion and lactic acidosis) include minimizing (1) the rate of additional blood loss, (2) hypothermia from the rapid intravenous administration of room temperature fluids, and (3) the dilution of blood hemoglobin and plasma coagulation factors.

However, on page 442 of Fischer's Master of Surgery, there is special circumstances related to secondary brain injury from edemafrom volume overload. (I am sure there is something in Miller's too, but I use multiple sources when possible)

I will not let me copy and paste the text, but it basically says overhydration must be avoided to prevent secondary injury from increased ICP.

In addition to the dozens of other sources I have followed this topic on, it seems very clear that a precision approach to volume resuscitation is the best option.

I would also stipulate that in hemorrhagic shock with TBI, the amount of permissive hypotension would be much lower than 90mmhg as even nephrologists I know consider 60mmhg over short periods to permit viability of the kidney.

 

[epipusher]

Agree with the tko rate and lowering the amount of O2 being given.

 

[rhan101277]

I lowered O2 to 6L NC in the truck, I put him on a NRB for a few minutes until I could do further assessment in the truck. Also a good pulse ox doesn't mean things are well, I had someone with a H&H of 3 and 10 and he had a pulse ox of 100%.

A 60mmHG systolic is strange considering a MAP of 60 is required for end organ perfusion. Seems like 60, for long periods, would lead to multi organ failure

 

[Dwindlin]

I lowered O2 to 6L NC in the truck, I put him on a NRB for a few minutes until I could do further assessment in the truck. Also a good pulse ox doesn't mean things are well, I had someone with a H&H of 3 and 10 and he had a pulse ox of 100%.

A 60mmHG systolic is strange considering a MAP of 60 is required for end organ perfusion. Seems like 60, for long periods, would lead to multi organ failure

No one is suggesting a pulse ox of 100% means everything is fine, but more FiO2 isn't going help that Hbg of 3...

I use lowest FiO2 to keep patient above 94%.

 

[Melclin]

I wouldn't have given this pt any fluid.

Oxygen via NC to high 90's. Two lines. Pain relief. Fent probably. See what effect both of those had on HR, but at the end of the day, I wouldn't give any fluid until his conscious state dropped off. If we were out in the boonies and things were going south, a chopper with some blood on it would be nice.

Saline doesn't clot and it doesn't carry oxygen. So we're really not doing much for them. You add that to the fact its probably going to make matters worse in terms of dilution coagulopathies.

I recently had a hypotensive pt who had experienced an episode of near syncope on exertion. Seemed like a combination of reflex mediated syncope exacerbated by dehydration and recent illness. She got 1.5 litres of NS targeting her normal BP. Turns out it was an upper GI bleed. She had a massive haematemesis and crashed shortly after. The saline's role in causing her to rebleed is interesting to think about. I took the case to the senior intensive care paramedic responsible for QA/QI and education and we had a good chat about what "judicious" fluid administration in the hypotensive GI bleed really means (our guidelines suggest 80-100 systolic but its just a suggestion on account of there not being a lot of evidence on the topic). We concluded that any fluid should be titrated to the resolution of any symptoms of that hypotension (in pleasant contrast to some of the stories I hear on this site, I was actually congratulated for stepping outside of the guidelines with a good justification despite the fact that I was ultimately wrong and probably worsened the pt's condition). At first my pt had a BP of 60/40, no radial pulses, nausea and was profoundly dizzy. Long transport time. Elderly. So fluid was indicated. The first 400mls NS alleviated her symptoms, saw the return of a radial pulse and took her BP to 90/50. Had I known she was having a GI bleed, I would have left it there.

Surely you don't have to give them the saline just because the protocols says so. I mean I'm down with the idea that you can't be doing things that aren't mentioned, but not doing something is different. It must be your choice whether or not you choose to apply the protocol in the first place.

 

[Veneficus]

A 60mmHG systolic is strange considering a MAP of 60 is required for end organ perfusion. Seems like 60, for long periods, would lead to multi organ failure

It is most often in the context of surgery, but is based on the length of time for the kidney to recover from ischemic injury without complete failure.

 

[OIFXGunner]

Just a couple of thoughts...

Cap refill is generally considered an unreliable indicator of perfusion in patient populations outside of infants and peds.

What was your transport time? Personally if I'm only 10, 15 mins away from the hospital, I'd be content with running a 250cc bolus or none at all because of how close I am and reevaluating that decision as I'm transporting.

Can you give a little more about the patient's hx?